Past and Present
John A. Jane, David Yashon, William DeMyer and Paul C. Bucy
Goro Tsuchiya, Oscar Sugar, David Yashon and John Hubbard
David Yashon, Alfred P. Magness II and W. Michael Vise
✓ The authors review the intraoperative use of elective hypotension to reduce the probability of hemorrhage, to increase pliability of the aneurysmal sac for ease of clip application, and to control hemorrhage. The optimum agent and techniques for lowering systemic blood pressure remain controversial, but trimethaphan, sodium nitroprusside, and halothane have been found most useful. When cerebral blood flow falls below the brain's capacity to autoregulate, distinct time-related alterations occur biochemically and histologically. The profile of prolonged reduced adenosine triphosphate (ATP), low phosphocreatine, low glucose, and elevated lactate and lactate/pyruvate ratio is associated with swelling of perivascular astrocytes and “blebbing” of vascular endothelial cells with subsequent cerebral damage. To prevent permanent alteration it is desirable to observe time constraints and to employ other means of protection such as hypothermia, although the authors believe the latter unnecessary for short hypotensive periods. It has been proposed, but not substantiated, that anesthetics which depress rate of cerebral oxygen consumption but do not affect cerebral ATP level protect the brain from hypotension. Several investigations suggest that halothane, a vasodiltor, satisfies the safety requirement. The most prominent contraindication to halothane, however, is elevation of intracranial pressure. At present hypotensive surgery for aneurysmorrhaphy is usually performed when intracranial pressure has returned to normal. Experimentally the electroencephalogram has been observed to show alterations prior to biochemical parameters for following brain vulnerability, so that it conceivably could be an effective monitoring technique during prolonged profound hypotension.
W. Michael Vise, David Yashon and William E. Hunt
✓ Vascularity and blood-brain barrier (BBB) function within spinal cord were studied with fluorescent microscopy at 14 intervals following 300 gm-cm injuries to the thoracolumbar spinal cord in 32 dogs. Histochemical staining with formaldehyde brought out a yellow-green fluorescence of vascular origin that was unrelated to tracer dye. This fluorescence accumulated in perivascular sites and is possibly related to catecholamine elevation within damaged spinal cord. Intrinsic CNS mechanisms for catecholamine build-up (increased transport, increased synthesis, increased release) are reviewed as well as the pharmacological action of alpha methyl tyrosine. It is hypothesized that an intrinsic CNS source of norepinephrine build-up is unlikely and that elevation of circulating catecholamine levels following stress and trauma leads to the extravasation of this material across injured BBBs within contused spinal cord.
Terifumi Ito, Norman Allen and David Yashon
✓ Cytochrome oxidase activities were determined by a microspectrophotometric method on microdissected samples of gray and white matter from frozen-dried sections of dog spinal cord. Experimental animals received 400 gm-cm impact at the T-3 to T-4 level. Sections for enzyme analysis and histological study were taken at the center of the trauma site, at successive 1-mm distances from the center, and at non-traumatized segments. A drop in cytochrome oxidase activities to approximately 50% of normal value was found as early as 15 minutes post-trauma, with greatest decrease at the trauma center and lesser effects at successive distances. This effect was related to known morphological defects in mitochondrial cristae and inner membranes. The enzyme change was significantly correlated with histological estimates of gray matter and neuronal damage, but was also partially independent of these processes. A small but significant increase of enzyme activity in white matter at the trauma site was considered most likely attributable to mitochondrial accumulations due to impaired axoplasmic flow.
David Yashon, George E. Locke and William E. Hunt
✓ Thirty-seven dogs were studied to establish the level of mean arterial pressure (MAP) causing cerebral tissue lactate (CTL) accumulation as a result of anaerobic metabolism and to assess the extent of preservation of aerobic metabolism afforded by autoregulation during oligemia. Specimens were removed prior to oligemia and at 5, 30, and 60 min following hypotension created by blood withdrawal. In four control animals, CTL averaged 4.83 (range 3.26 to 7.07) mMol/kg. At 60 min after induction of oligemic hypotension, 13 animals with a MAP of 30 and 40 mm Hg showed concentrations of CTL between 16.56 and 20.89. At a MAP of 50 mm Hg six animals showed a CTL concentration between 4.39 and 15.88; at a MAP of 60 mm Hg eight animals showed a CTL between 3.76 and 14.93; and at a MAP of 70 mm Hg six animals had a CTL between 2.43 and 4.27. At 5 min, at all mean arterial pressures the cerebral tissue lactate varied between 2.07 and 5.50. By 30 min the elevations were similar to those at 60 min. CTL elevation was independent of pre-oligemic MAP. In the canine brain there is a uniform incremental elevation of CTL between a MAP of 30 to 50 mm Hg directly related to the time of hypotension; there is variable intolerance to MAP in the range of 50 to 70 when related to a time longer than 5 min.
Jane C. S. Perrin, Martin H. Weiss and David Yashon
✓ A family with craniofacial dysostosis affecting a father and his monozygotic twin sons is described. The father had no surgery until linear craniectomy when 3 years old; he is of normal intelligence but legally blind. Prophylactic coronal craniectomy and orbital decompression were done on the twins. One had an uncomplicated course and is developing normally. The other developed neonatal meningitis and ventriculitis with secondary hydrocephalus, plus poor vision and retarded development.
David Yashon, W. Michael Vise, Richard C. Dewey and William E. Hunt
✓ The temperature of the spinal cord parenchyma during local hypothermia was recorded in 18 dogs with and without a 300 to 500 gm-cm spinal cord injury. Other variables included opening the dura, location of the inflow stream, and the use of alcohol bath cooling. In nontraumatized cord, the temperature varied between 5.4° and 23.5°C depending on the location of the inflow stream; the variable range of 10–15 minutes of perfusion to reach these levels was unexpected. Temperatures of the injured cord fell to those of the reservoir (1.0° to 3.8°C) within 2½ minutes. The fact that the temperature of nontraumatized areas two segments cephalad to the injury was also reduced showed the capacity of the cord for thermal conduction. Opening the dura or use of an alcohol bath had little effect on cord temperature. Lack of heat transport due to ischemia is postulated as the primary cause of the rapid reduction of temperature in the injured cord to that of the surrounding environment.
David Yashon, W. George Bingham Jr., Edward M. Faddoul and William E. Hunt
✓ Identification of central nervous system edema is based on increased water content in relation to nonvolatile residue per unit weight. Nonvolatile residue in spinal cord tissue following impact trauma was determined to ascertain the magnitude and persistence of edema. High and low thoracic laminectomies were carried out on each of 17 rhesus monkeys. The lower exposed cord was traumatized with a calibrated blow of 300 gm cm. All upper exposed cords and the lower exposed cord in one monkey served as nontraumatized controls. At time intervals of 5 minutes to 20 days after trauma, cord segments were removed and assayed for water content. Increased tissue water was evident within 5 minutes and persisted for 15 days. By the 20th day it had essentially subsided. Increased tissue water content in the traumatized segment reached a maximum of 7.4% over control values at 5 days and then gradually diminished. These findings support the concept that edema following spinal trauma is unrelated to secondary effects of ischemia after 18 hours. The protracted course of increased water content (15 to 20 days) was unexpected and may indicate that edema-reducing measures should be continued for 2 to 3 weeks following spinal cord trauma with severe neurological dysfunction.